The blog tries to link the research to the currently popular "
ischemia-reperfusion hypothesis", which proposes that PEM is caused by improper blood flow:
The study used a technique called “flow-mediated skin fluorescence (FMSF) which the authors stated was “uniquely suitable” for assessing the microcirculation during periods of low blood flow (transient ischemia). A recent hypothesis proposed that people with long COVID or ME/CFS were in a chronic state of transient ischemia due to inadequate blood flows.
Putting aside the fact that "chronic transient ischemia" is an oxymoron, the "ischemia-reperfusion hypothesis" is indeed a popular theory right now due to interest in the cardiovascular manifestations of a coronaviral infection. However, upon further inspection, this theory falls flat.
Specifically, the symptoms of PEM are nothing like the symptoms of ischemia-reperfusion injuries. Whereas PEM symptoms are generalized and varied, ischemia-reperfusion injuries tend to produce localized, well-defined symptoms.
For example, ischemia-reperfusion injuries in limbs can produce myalgia and paresthesias, which is something like Delayed-Onset Muscle Soreness (DOMS) with Peripheral Neuropathy (PN). Inflammation markers in such ischemia-reperfusion injuries would likely be elevated, whereas inflammation markers in PEM are not reliably elevated.
An ischemia-reperfusion injury to the brain would produce stroke-like symptoms, essentially a Transient Ischemic Attack (TIA). Although cognitive exertion can trigger PEM, it is not at all clear how cognitive exertion could produce a TIA.
So really, PEM is nothing like ischemia-reperfusion injuries.
